Monday, March 25, 2019

In my case this was a collection of mistakes,misstatements and falsehoods all neatly printed out in a manner that may facilitate the physician getting credit for various quality measures. After reading the AVS I asked myself do I really want a serious medical problem that I may develop to be overseen by someone who signs off on such a pile of crap.

Several aspects are worth a blog entry. Today it is the "After visit Summary" (AVS) which was available the next day on the practice's web site .Actually it is the hospital web site's patient portal,
This group of internists is "hired" by the hospital under the guise of being a practice group somehow affiliated with the hospital.Remember there previously was something call the Corporate Medicine Doctrine.

My particular AVS is a sleek , multicolored document replete with little icons by such entries as your weight (icon of a dial),pulse ( icon of a valentine style heart). etc.

Under "Today's Visit" we see small head shot photo of the physician and a listing of the addressed issues.This was a collection of mistakes,misstatements and outright falsehoods which are now part of my permanent record.

I was said to have atrial fibrillation. I do not have AF. The diagnosis of AF was erroneously placed on the chart by the EP clinic but was later ( 8 months) corrected and removed from my problem list. I mentioned to my PCP that do not have AF and that the earlier entry was the results of a error in the EP clinic.This was the second time I explained about the diagnosis of AF to him and his scribe with no effect on my permanent record.

I was also said to have "osteopenia of both hips" .WTF. I have had no imaging of my back or hips at that facility .

I was said to have "hypercalcemia" and "hypergammaglobulinemia "When first seen by this PCP one issue was a metabolic profile done by my previous PCP that was stuffed with errors, namely elevated, calcium,elevated K and elevated globulin ( all likely the results of hemolyzed blood sample). These were all repeated and found to be normal but some how the diagnosis of hypercalcemia and elevated globulin level remain.

Nevertheless, on my AVS I was told that those issues were addressed.

What is the AVS all about? it is about "meaningful use".It is one of the eligible professional meaningful use core measures. It all began in 2009 with the HITECH act that was designed to "encourage physicians" to use an EHR.There were monetary carrots and sticks. Neither of which seem to me to be much more than chump change particularly after considering the care and feeding of a EHR .

Kaiser Health News and Fortune Magazine have a detailed article describing what a utter disaster the EHR has become.The title is "Death by A Thousand Clicks".

Here are some of the highlights and the entire article by Mandrola (full text is available) is recommended.

Aspirin is no longer recommended for low risk AF patients. As Mandrola says , just like that, without much of an explanation .

Both the FDA and CMS have approved percutaneous left atrial appendage closure with the Watchman device and the panel gives it. a class 11b recommendation. Apparently, the panel did not see fit to comment on the 4% risk of device associated thrombosis reported with Watchman.

DOACs now is officially preferred over warfarin. Not mentioned by Mandrola is the observation that the fewer strokes with DOACs versus warfarin is driven by the fact there are fewer hemorrhagic strokes with DOAC while there is little if any difference in the number of ischemic strokes.

The task force stated that female sex alone is no longer considered a risk factor for stroke in an AF patient per se.

The guideline writers gave a class 11 b (additional studies are needed-procedure may be considered) recommendation for AF ablation in heart failure.Mandrola believes the data supporting AF ablation in HF patients is sufficient for the panel to have given a higher recommendation quoting the positive results of the CASTLE-AF trial that showed a 12% absolute risk reduction in death and in heart failure admissions in the ablation cohort.

Mandrola shares my views on the CHA2DS2VASc score . It is "simple to use , but at its core distills a decidedly continuous risk for a future event down to an integer." He references D. R. Quinn's 2017 review of 34 studies of AF ( reference can be found in Mandrola's review) that illustrate the large variation in the baseline risk of stroke in untreated AF patients. Quoting Mandrola " Translation: We have no idea of the risk in untreated patients.",and yet every day cardiologists and other docs crank out the CHA2DS2VASC and mater-of-factly tell their patient that they have x% annual risk of stroke and suggest how much that risk will be reduced by oral anticoagulation."

I have written about Quinn's study before and quoting from Quinn's article "'
The majority of cohorts did not observe stroke rates that would indicate a
clear expected net clinical benefit for anticoagulating AF patients
with a CHA2DS2-VASc score of 1 or 2."

Monday, March 11, 2019

Left anterior fascicular block (LAFB) was previously known as left anterior hemiblock (LAH) .The earlier designation can be attributed to the widely accepted writings of Maurico Rosenbaum whose work ( 1967) seemed to indicate that in humans the left bundle divided into a left and a right branch.

This "trifascicular" concept (right bundle branch and the two branches of the left bundle) was widely accepted and persisted even though work in 1972 by Demoulin and Kulbertus make it clear than there was also frequently a septal branch of the left bundle and more importantly that the anatomy of left bundle is much more complex that simply consisting of two (or three) branchs, i.e. more of a spiderweb or fan.There is great variation in the interconnections and in only few of the 49 careful dissections by Demoulin can a simple pattern of 2 or even 3 fascicles be seen. (the patterns can be seen on page 283 of reference 1, full text is available)

Realizing that all models are wrong but some are useful ( George Box, circa 1978),it may be that the LAFB model has some value.

LAFB is diagnosed on EKG when the frontal plan axis is between minus 30 and minus 90 with QRS duration less than 120 msec and the patient does not have an inferior wall myocardial infarction,LVH or WPW syndrome.So, typically LAD equals LAFB in the EKG reading context.

Mandyam et al ( 2) from UCSF studied long term outcomes in patients with LAFB who at the beginning of the data collection did not have evidence of heart disease. Using data from the Cardiovascular Health Study (CHS), they compared 39 subjects with LAFB with 1625 patients without LAFB over a 19 year period.The average age of the control groups with 71.4 and the age of LAFB group was 74.9

They report LAFB was significantly associated with atrial fibrillation (AF) Heart failure(CHF) and death with the following p values-AF .02,CHF .02, and death .001.

This was a small ( 39 patients),coarse grain study.The authors point out that although CHS tries to exclude preexisting disease on entry to the program hypertension or asymptomatic coronary artery disease may have been missed. The authors referenced no corroborating studies .

This UCSF article received considerable medical press coverage in part as it offered some suggestion that the previously accepted notion that LAFB was a "benign" finding might not be correct but within a year their findings were seeminly contradicted by research from Copenhagen.

JB Nielsen (4) studied the cardiovascular outcome of 222,227 subjects with a 5.7 year follow-up period. They did find a statistically significant correction between LAFB and AF, HF and both all cause and cardiovascular mortality. However, after adjusting for age and gender only the all cause risk retains statistical significance.

Quoting the authors: "current EKG definition of LAFB is not always clinically important marker of cardiovascular morbidity and mortality beyond what can be expected by age and sex."

What is the effect of LAFB on left ventricular function?

Leeters and colleagues from The Netherlands studied 28 patients with RBBB,LAFB and heart failure with 2D speckle tracking regional strain measurements as well as healthy controls and 28 LBBB patients. This is not a study of "lone LAFB" as the patients had RBBB and HF and a number of them had scars detected by CMR. Since the RBBB per se would not affect Left ventricular activation sequence it is reasonable to assume the delay in activation of the anterior LV is due to the LAFB.The study indicated wall motion abnormalities between the anterior wall and inferior wall of the LV analogous to the classic pattern of septal and lateral LV wall dyssynchrony characteristic of LBBB but apparently less disruptive of cardiac function.